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- •Contents
- •Contributors
- •Abbreviations
- •Foreword
- •Introduction
- •(Very) brief history of IAP
- •Further reading
- •Introduction
- •Background
- •The abdominal wall
- •The relation between IAP and IAV – compliance and elastance
- •Key points
- •Key points
- •Further reading
- •Measure IAP at the end of expiration
- •IAP is (usually) measured in the bladder
- •IAP can be measured through routes other than the bladder
- •IAP can be measured with fluid-filled or air-filled systems
- •IAP should be measured against a reference level
- •Instillation of fluid in the bladder is required
- •The temperature of the instillation fluid should be controlled
- •The patient’s body position is important
- •Supine versus semi-recumbent position
- •Prone position
- •Other positions
- •The effect of positive end expiratory pressure (PEEP) on IAP
- •Key points
- •Further reading
- •Introduction
- •Clinical estimation of IAP
- •Measurement of IAP is safe
- •Measurement of IAP is reproducible
- •Routes for IAP measurements
- •Transvesicular route
- •Transgastric route
- •Alternative routes
- •Modalities of IAP measurements
- •Available methods for IAP measurement
- •Intermittent IAP measurement
- •Transvesicular: Harahill method
- •Transvesicular: AbViserTM IAP Monitoring Kit
- •Transvesicular: Bard IAP® Monitoring Device
- •Transvesicular: Biometrix
- •Transvesicular: PreOx IAP Adapter
- •Transgastric: gastric tube or Collee method
- •Transgastric: gastric balloon method
- •Continuous IAP measurement
- •Continuous transvesicular IAP measurement
- •Continuous IAP monitoring – CiMON (Pulsion Medical Systems)
- •The IAP-Catheter and IAP-Monitor (Spiegelberg)
- •Key points
- •Further reading
- •Introduction
- •The pitfalls
- •Pitfalls related to the patient
- •Positioning of the patient
- •The awake patient
- •Intra-abdominal space-occupying lesions
- •Obesity
- •Children
- •Pitfalls related to the measurement technique
- •Zero reference level
- •Gastric route
- •Infusion volume
- •Infusion temperature
- •Frequency of IAP measurement
- •Pitfalls related to the interpretation of data
- •Key points
- •Further reading
- •What is abdominal compliance?
- •Why is abdominal compliance important?
- •Implications for clinical practice
- •How does decreased abdominal wall compliance lead to IAH?
- •Is this clinically important?
- •Can I and should I measure abdominal compliance in my patient?
- •How do I know when abdominal wall compliance is decreased?
- •How do I know when abdominal wall compliance is increased?
- •Key points
- •Further reading
- •Introduction
- •Measuring IAV
- •IAV in clinical practice
- •Is IAV relevant?
- •IAV and primary IAH
- •IAV and secondary IAH
- •Other ways in which IAV has an impact on IAH
- •Key points
- •Further reading
- •Introduction
- •Capillary dynamics
- •Capillary leak in the critically ill patient
- •IAP and the three hits model of shock
- •The ebb phase
- •The global increased permeability syndrome
- •Consequences of IAH and ACS in the patient with severe acute pancreatitis
- •When it starts to get better (day 3)
- •Key points
- •Further reading
- •Introduction
- •Why and when do patients with severe acute pancreatitis develop IAH and ACS?
- •Diagnosis of IAH and ACS in the patient with severe acute pancreatitis
- •Prevention of IAH and ACS in the patient with severe acute pancreatitis
- •Treatment of IAH and ACS in the patient with severe acute pancreatitis
- •Surgery
- •Feeding
- •When can the clinician stop considering IAH in patients with severe acute pancreatitis?
- •Key points
- •Further reading
- •Introduction
- •IAP in children
- •Normal values of IAP in children
- •Measurement of IAP in children.
- •Outcomes of IAP in children
- •IAH and ACS in children
- •Diagnosis of IAH and ACS in children
- •Management of IAH and ACS in children
- •Key points
- •Further reading
- •Introduction
- •Types of ACS in trauma patients
- •Incidence
- •The ‘bloody’ vicious circle and IAH
- •Conservative management of the patient with abdominal trauma
- •IAH in the patient with an open abdomen
- •Key points
- •Further reading
- •Introduction
- •Incidence
- •Consequences of IAH in the patient with severe burns
- •Monitoring IAP in the burn patient
- •IAH prevention in the burn patient
- •Urine output as an indicator during resuscitation of the burn patient
- •Treatment of IAH in the burn patient
- •Key points
- •Further reading
- •Introduction
- •Normal values of IAP in obese patients
- •IAP and chronic morbidity in the obese patient
- •Systemic hypertension
- •Pseudotumour cerebri
- •Respiratory morbidity
- •Incisional hernia
- •Key points
- •Further reading
- •Introduction
- •Pregnancy and IAP
- •Peritoneal dialysis and IAP
- •IAP during iatrogenic pneumoperitoneum
- •IAP in the haematological patient
- •Any other conditions leading to IAP?
- •Gastroenterology
- •Respiratory
- •Neurology
- •Cardiology
- •Gynaecology
- •Reconstructive surgery
- •Orthopaedics
- •Miscellaneous
- •Key points
- •Further reading
- •Introduction
- •Pathophysiology
- •Overall cardiovascular effects of IAH
- •IAH and preload
- •IAH and contractility
- •IAH and afterload
- •Implications for clinical practice
- •Filling pressures are inaccurate with IAH
- •What about volumetric monitoring?
- •Abdominal perfusion pressure (APP)
- •IAP and responsiveness to fluid
- •Key points
- •Further reading
- •Introduction
- •IAH and acute lung injury
- •IAH and lung distension
- •IAH and pulmonary oedema
- •IAP and mechanical ventilation
- •IAP and pulmonary hypertension
- •Key points
- •Further reading
- •Introduction
- •Incidence
- •Critical IAP in relation to renal function
- •The impact of IAH-induced kidney failure
- •Implications for clinical management
- •Diagnosis of AKI in patients with IAH?
- •Prevention of IAH-induced kidney injury?
- •How do I treat the patient with IAH-induced AKI?
- •Key points
- •Further reading
- •Introduction
- •How does IAH lead to intracranial hypertension?
- •Importance of the impact of IAH on ICP
- •Conditions associated with increased IAP and ICP
- •Implications for clinical management
- •Prevention of IAH-induced raised ICP
- •Treatment of IAH when ICP is raised
- •Key points
- •Further reading
- •The liver and IAH
- •Gastrointestinal function and IAH
- •The abdominal wall and IAH
- •Endocrine function and IAH
- •Key points
- •Further reading
- •Introduction
- •Multiple organ dysfunction syndrome
- •IAH as a marker of gastrointestinal dysfunction
- •Implications for clinical practice
- •Key points
- •Further reading
- •Introduction
- •Abdominal compartment syndrome
- •Other compartment syndromes
- •Hepatic compartment syndrome
- •Renal compartment syndrome
- •Pelvic compartment syndrome
- •Cardiac compartment syndrome
- •Intracranial compartment syndrome
- •Intraorbital compartment syndrome
- •Limbs or extremity compartment syndrome
- •Polycompartment syndrome
- •Key points
- •Further reading
- •Decreased abdominal wall compliance leads to IAH
- •Measuring abdominal compliance
- •Preventing decreased C-abd
- •Increasing abdominal wall compliance
- •Key points
- •Further reading
- •How do intraluminal contents lead to IAH?
- •Ileus and IAH
- •Enteral feed
- •Evacuation of intraluminal content
- •Surgical intervention
- •Key points
- •Further reading
- •Introduction
- •What are the causes of abdominal fluid collections leading to IAH?
- •What about more factors leading to IAH or ACS?
- •Implications for clinical management
- •Do all fluid collections require drainage?
- •How to drain abdominal fluid collections safely?
- •Which catheter should be used for draining fluid collections leading to IAH?
- •When is PCD to be avoided?
- •When does the patient need a (decompressive) laparotomy?
- •Key points
- •Further reading
- •Introduction
- •How does systemic inflammation lead to (secondary) IAH?
- •Incidence
- •Consequences of secondary IAH
- •Implications for clinical management
- •How to prevent development of secondary IAH?
- •What are the possible interventions for capillary leak syndrome?
- •How is capillary leak prevented or diminished?
- •How are fluids used in the patient at risk for IAH?
- •How is volume status and fluid responsiveness assessed in patients with IAH?
- •What fluids to use?
- •How is fluid overload associated with secondary IAH treated?
- •Key points
- •Further reading
- •Introduction
- •Octreotide in IAH
- •CNAP devices
- •Traditional Chinese medicine
- •Melatonin treatment
- •Nutrition
- •Key points
- •Further reading
- •Introduction
- •Can abdominal decompression treat ACS?
- •Is surgical decompression safe?
- •Surgery is for all patients
- •What surgical methods can be applied?
- •Should abdominal decompression be the only cure for ACS?
- •Implications for clinical management
- •When should surgical treatment be considered?
- •Can abdominal decompression be performed in the ICU?
- •What are the pitfalls when decompressing the abdomen in ACS?
- •Is decompression an option when only IAH is present?
- •Does every patient require TAC after decompressive laparotomy?
- •Key points
- •Further reading
- •Introduction
- •Characteristics of an ideal TAC
- •Negative pressure therapy measures
- •Implications for clinical management
- •What TAC technique is to be preferred?
- •Where to change the TAC
- •When to change the TAC
- •When to remove the TAC
- •Temporary abdominal closure techniques
- •Skin closure-only TAC
- •Synthetic cover-only TAC
- •Negative pressure TAC
- •Fascial approximation techniques
- •Key points
- •Further reading
- •Natural history of IAH shows that short-lived IAH can be tolerated by some patients
- •Continuous, hassle-free IAP measurement makes recognition of the problem easy
- •Prevention is better than therapy
- •Medical management is the gold standard for IAH
- •Decompressive laparotomy will no longer be a therapy for ACS
- •Open abdomen therapy is used selectively in the high-risk patient and for the shortest time possible
- •Epidemiology
- •Index

Chapter 10: Children 105
Key points
Normal IAP in mechanically ventilated children is about
7 mmHg.
Critical values of IAP that suggest IAH and ACS are lower in
children.
In children, IAP greater than 10 mmHg should be
considered to be IAH.
IAP above 10 mmHg associated with new organ dysfunction
is ACS in children until proven otherwise.
Abdominal breathing in children may result in erroneous IAP
readings.
FURTHER READING
Ejike JC, Bahjri K, Mathur M. What is normal intra-abdominal
pressure in critically ill children and how should we measure
it? Critical Care Medicine 2008; 36: 2157–62.
Ejike JC, Humbert S, Bahjri K, Mathur M. Outcomes of children
with abdominal compartment syndrome. Acta Clinica
Belgica Supplement 2007; 1: 141–8.
Ejike JC, Kadry J, Bahjri K, Mathur M. Semi-recumbent position
and body mass percentiles: effects on intra-abdominal
pressure measurements in critically ill children. Intensive
Care Medicine 2010; 36(2): 329–35.

Chapter 11
Trauma
Introduction
Occurrence of ACS is not limited to abdominal trauma patients.
Secondary ACS can be a frequent complication in severely
injured patients if IAH is not prevented. All patients sustaining
severe trauma, irrespective of its location, are at risk of
developing IAH and ACS. Prevention of secondary ACS is
possible by the application of ‘damage control’ surgery,
judicious fluid resuscitation and adherence to specific
transfusion protocols.
In patients requiring ‘damage control’ surgery, leaving the
abdomen open is a key element in preventing ACS. When
ACS develops in trauma patients, early decompression is
advised. After decompression, non-surgical measures will allow
early abdominal closure.
Organ dysfunction is a marker of development of IAH
and ACS.
Types of ACS in trauma patients
Both primary and secondary ACS are commonly seen in
trauma patients.

Chapter 11: Trauma 107
The usual presentation of primary ACS is severe abdominal
trauma requiring ‘damage control’ laparotomy with (or
without) packing and abdominal closure. While the abdominal
trauma is the direct cause, mechanisms leading to secondary
ACS such as fluid resuscitation contribute to further
deterioration.
All types of extra-abdominal trauma can lead to secondary
ACS. Secondary ACS usuallydevelops later than primary ACS but
should be considered at any time if organ dysfunction develops.
This may happen within the first 12 hours after injury, and
IAP monitoring is always indicated in severely injured patients.
Incidence
The incidence of IAH and ACS in trauma patients is decreasing
rapidly as centres have embraced these concepts and apply
strategies that avoid the occurrence of both primary and
secondary ACS. A few years ago, the incidence of ACS was as high
as 40% with high mortality rates. It has reduced dramatically
in recent years. The occurrence of ACS in trauma patients is now
considered an indicator of suboptimal trauma care.
The ‘bloody’ vicious circle and IAH
The ‘bloody vicious cycle’ or ‘lethal triad’ of trauma patients is
the combination of coagulopathy, hypothermia and acidosis.
These three factors contribute to ongoing blood loss from
the injured body. Ischaemia/reperfusion injury occurs at the
initiation of resuscitation.

108 Section 3: Specific conditions: when to worry more?
Early control of blood losses and restoration of the
coagulation capabilities of the blood are important in avoiding
this lethal triad. Resulting oedema (inside and outside the
abdominal cavity) will result in IAH. Strategies aimed at
preventing this lethal triad will effectively prevent ACS.
‘Damage control’ surgery aims at early and rapid control of
blood loss. Prophylactic open abdomen management is an
early step. Rapid transfer of the patient to an intensive care
unit to correct acidosis, hypothermia and coagulopathy is
essential. Definitive repair of non-life-threatening injuries can
be delayed to a later stage.
It is often difficult to distinguish ACS from shock, continuous
bleeding and related inflammatory responses. To help
differentiate between these, IAP measurement is required early
in trauma patients.
Predicting factors of IAH in the trauma patient are shown in
Table 11.1.
Table 11.1 Predictors of ACS in trauma patients
Primary ACS Secondary ACS
Temperature <34°C Administration of >7.5 L of crystalloids before
ICU admission
Haemoglobin <8 g/dL No indication for life-saving surgical intervention
Base deficit >8 mmol/L Relatively low urine output (<50 mL/h)
Administration of >3 L of
crystalloids
Transfusion of ≥3 units of
red cells
Need for emergency surgery
Poor intestinal perfusion measured by gastric
tonometry

Chapter 11: Trauma 109
Conservative management of the patient with abdominal trauma
Conservative management of the trauma patient does not
mitigate the risk of IAH and ACS. Patients may have lost
considerable amounts of blood in the peritoneum, and other
factors (such as oedema formation due to shock from
extra-abdominal injuries or ileus) may contribute to the
development of IAH. These mechanisms explain why IAH can
happen in patients treated with angiographic embolization.
Laparotomy is the definitive treatment option if residual
bleeding from the initial injury persists. Reports of successful
percutaneous drainage using large bore catheters are
encouraging.
Similar to patients with severe acute pancreatitis, trauma
patients who develop secondary ACS may benefit from a
subcutaneous linea alba fasciotomy (SLAF). This is an attractive
alternative in patients who did not require an initial
abdominal surgical intervention.
IAH in the patient with an open abdomen
The risk for ACS in patients with an open abdomen is low but
new issues (such as bleeding) may lead to an increase in IAP.
A midline laparotomy may be inadequate (too small) to
decompress the abdomen fully.
Moreover, IAP can decrease after abdominal decompression
but still remain above the threshold for continued damage to
various organ systems. Medical strategies to decrease IAP

110 Section 3: Specific conditions: when to worry more?
further are important to reverse organ dysfunction. An open
abdomen is just one element in the treatment, and does not
preclude the development of IAH and ACS.
The abdomen should remain open as long as this benefits the
patient, but attempts should be made to close the abdomen
early. A fine balance is required. Continued IAP measurement
is indicated to help make the right decision.
Key points
IAH and ACS can occur both in abdominal trauma and
extra-abdominal trauma patients.
Patients at risk for IAH should be identified at an early stage of
their treatment.
IAP must be measured regularly in all severely injured
patients irrespective of the site of injury.
Early bleeding control and avoiding massive transfusion are
key elements in preventing IAH in trauma patients.
Open abdomen treatment should be applied liberally in
patients at risk.
The use of medical management strategies to reduce IAP
will facilitate early closure of the abdomen, and avoid
complications related to open abdomen treatment.
FURTHER READING
Ball CG, Kirkpatrick AW, McBeth P. The secondary abdominal
compartment syndrome: not just another post-traumatic
complication. Canadian Journal of Surgery 2008; 51: 399–405.

Chapter 11: Trauma 111
Cheatham ML, Safcsak K. Is the evolving management of
intra-abdominal hypertension and abdominal compartment
syndrome improving survival? Critical Care Medicine 2010;
38: 402–7.
Rizoli S, Mamtani A, Scarpelini S, Kirkpatrick AW. Abdominal
compartment syndrome in trauma resuscitation. Current
Opinion in Anaesthesiology 2010; 23: 251–7.

Chapter 12
Burns
Introduction
Severe burn patients develop IAH/ACS within 48 hours.
The increase in capillary permeability contributes to
extensive oedema formation and intraperitoneal
accumulation of fluid. Gut oedema and fluid translocation
is worsened by venous hypertension caused by an
elevated IAP.
Figure 12.1 shows the relationship between the
resuscitation fluid volume received within the first 24 hours
of the insult, the percentage of the total body surface area that
has been burned and ACS.
Secondary ACS in burn patients generally occurs within
48 hours of the injury, during the initial resuscitation
period. The risk decreases substantially when the patient
reaches the ‘diuretic phase’. The risk for IAH/ACS increases
again if the patient develops sepsis.
Incidence
The incidence of IAH depends on the severity of the burn
injury. The risk of ACS is directly related to the burned area.

Intravenous Fluid Volume (mL/Kg/24h) Total Body Surface Area (%)
600
500
400
300
200
100
0
50
100
Figure 12.1
Chapter 12: Burns 113
Individual Case
Consequences of IAH in the patient with severe burns
IAH is associated with impaired organ dysfunction, including
the cardiovascular, respiratory and renal systems. In severe
burn patients, the kidneys become vulnerable and preserving
renal function is particularly important. ACS alone, or when
associated with its surgical treatment, increases the risk of
multiple organ dysfunction, including acute lung injury. The
mortality rate of patients developing ACS is 50–80%, even
when treated.

114 Section 3: Specific conditions: when to worry more?
Monitoring IAP in the burn patient
IAH/ACS should be considered in all patients with severe
burns. IAP measurement should be performed every 2–4 hours
throughout the resuscitation period in burn patients with more
than 20% of their body area affected.
IAH/ACS might occur in patients without circumferential
third degree burn of their trunk. Figure 12.2 shows a patient
with a tense abdomen despite normal elasticity of the
abdominal wall. Measurement of the IAP revealed a pressure
of 60 mmHg.
Figure 12.2
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